The mechanisms responsible for the pulmonary gas exchange effected by application of small tidal volumes (on the order of anatomic dead space or less) at high frequencies (HFV) (usually greater than 1 Hz) are not well understood. Although a general class of mechanisms (augmented dispersion) can possibly explain the gas transport achieved in this setting, clearer definition of how other factors influence the general mechanisms would be of value in the most rational application of this ventilatory strategy to patients with a variety of lung diseases. In this project we propose to combine engineering studies of hardware and computational models with physiological experiments in dogs (with normal and abnormal lungs) in order to determine how specific physical mechanisms control and limit pulmonary ventilation by HFV. Specifically, we propose to determine the extent to which each of five distinct mechanisms may operate to alter HFV efficacy. These mechanisms include: 1. Alteration of HFV mediated gas transport by the bias flow rate, 2. Alteration of HFV mediated gas transport by bias flow turbulence, 3. Ventilation of nearby alveoli, 4. Effects of compliant airways on HFV mediated gas transport, and 5. Effects of gas transport resistances in the alveolar zone. Although each mechanism will be addressed through distinct experiments and modeling studies, the results will be integrated into an overall computational model for HFV.